Great. Great. Thanks so much, Nishanta. I'm very happy to be here today and talk to you about a challenging topic. We've got a lot of cases that I hope will illustrate some of the difficulties with this problem. So we'll start with a case, a 52-year-old man with no past medical history who presented with syncope at a construction site where he works. He was evaluated at an outside facility initially, and he had an echocardiogram that just showed a low normal ejection fraction, 50% to 55%. And a CTA showed no obstructive coronary disease. They brought him for an EP study. And I think one of the first things that you'll notice, this is his baseline electrocardiogram. And you'll notice that his baseline ECG is not that normal. He's got a little bit of a right bundle. He's got a little bit of a left axis. And he's maybe got a touch of PR prolongation. And then when they put their catheters in for their initial risk-stratifying EP study, they measured his HV. And you can see that here is measured at 77 milliseconds, so a little bit prolonged. And they did program stimulation. So they induced VT with programmed extra stimuli. Actually, just with, in this case, two extra stimuli from the right ventricle, they were able to induce this sustained VT that you see here that's monomorphic. And so the first question I have for folks is what is your likely site of origin or exit of this tachycardia? And I have some options there. Interesting. Lots of different responses. I'm just watching the rates go. I don't know if we have to let it go the whole time. You can stop it whenever you want to, Nishant. But you can see there that we have most people voting for the right ventricular outflow tract, which I think is pretty consistent with what we see here. Let me close that for just a moment. You can see that there's a left bundle branch block configuration. There's inferiorly directed QRS complex in two and three. The transition is a bit late, V3 to V4. And we're negative in lead one. So that would kind of put you in, if we look at sort of a model of the heart with the ECG electrodes attached to us, that would put us sort of in the right ventricle, maybe the leftward part of the right ventricle. Pretty leftward given how negative lead one was. Some of the other answers that weren't terrible is the right coronary cusp is not far from this area. It could be just back here. You'd usually expect a bit of an earlier transition if it was going to be over that way. So that's sort of what we found, what they found on their initial EP study. So I think the question is here, does he need an ICD? And I think here's our potential answers. Oh, it's like a horse race watching this thing. It's like half and half, half and half. All right, we can stop that. That's great. So we're really pretty split evenly on the answers for that. So I think one of the things to keep in mind is when we think about idiopathic VT and ablating idiopathic VT, we're usually talking about somebody who has a normal baseline electrocardiogram and a normal echo. And so this guy has a normal echo, but his baseline ECG is pretty abnormal. And he's got a prolonged HV interval. And so that really warrants us thinking about him maybe a little bit more before recommending that he go without an ICD or that we implant an ICD. So because of his young age and the HV prolongation and the mechanism of the VT2, it was inducible with programmed stimulation rather than burst pacing, which may be a little bit more simple. Which may be a little bit more suggestive of a re-entrant mechanism. They've decided to do an FDG PET and an MRI. And they were able to identify a scar in the antireceptal distribution with edema consistent with active cardiac sarcoidosis. So at the other hospital that he received an ICD and immunosuppressives. And unfortunately over that year, despite the immunosuppressives he developed, he progressed to complete heart block, was upgraded to a CRTD device and had difficulties with symptomatic VT. And he was ultimately referred to us for catheter ablation. So I just wanted to spend a moment just reviewing some of the things that I think that Dr. Stevenson spoke about last week when he talked about VT and non-ischemic cardiomyopathy. This is some work from Katja Zeppenfeld's group where they looked at folks with non-ischemic cardiomyopathy and looked at patterns of scar. And here you can see that they grouped them into antireceptal scars and inferolateral scars. And the inferolateral scars were more often accessible from the epicardium or required epicardial ablation for termination of VT. But the septal scars were a bit more challenging. So if we think about these antireceptal scars, where are they located? They're sort of between the outflow tracts. They can involve the parahysian area. It's not unusual to get left bundle and right bundle types of VTs that we can see. Epicardial ablation is usually not helpful because of the location. There's often coronaries nearby. There are places where the myocardium is very thick and the myocardium can be bounded by septal walls on either side. There's also a risk of AV block from ablation. So when you're looking at folks with this kind of substrate, you want to be aware that that could be a problem. There are particular diseases that it should make you think of. So sarcoidosis, this was the case for this gentleman, but there are also a bunch of inherited cardiomyopathies that also can present with antireceptal scars. Lamin-AC cardiomyopathy is probably the prototype for that, but there are others such as phospholamban mutations. Some of the ARVC variants with biventricular involvement can have conduction system disease as part of their presentation. And here's just a couple figures from a paper that we published on a series of patients with cardiac sarcoid. And we think of these patients as having right ventricular cardiomyopathy very often as shown over here on the right side. You can see a right ventricular map, voltage map with low voltage areas sort of all around the annulus, also involving the septum, but involving the free wall too, just as you might see for arrhythmogenic right ventricular cardiomyopathies. But in addition to that, we often see that the parahysian area is involved. This is a left ventricular voltage map and you can kind of see where the his potentials are marked in yellow here and where the ablation for the VTs had to be. And you see a low voltage area that goes right around the aortic valve area in some of these folks. This is another series that we published looking at lamin cardiomyopathy. And just to remind you, this is a sort of a triad of patients with atrial arrhythmias, usually atrial fibrillation and AV block, as well as ventricular tachycardia that's monomorphic. And these are just a distribution of where we found VTs in these folks with lamin cardiomyopathy that went for VT ablation in a multicenter series. And this is the left ventricle sort of opened up and we're looking at that same periaortic septal area here. The darker areas were where the VTs were more frequently found and the lighter areas where they were less frequently found. So you can see that that same little area is the area that was involved in a lot of these patients. And you could identify a low voltage area from the right ventricle as well, sort of mirroring what was seen in the left ventricle. So when we brought this patient to our EP lab, it was very similar to what you would have thought based on what I just said. So we could induce the original VT that they saw at the outside hospital. But with program stimulation, we could also induce a second faster VT. And this actually matched at least on the basis of cycle length and electrogram morphology. More closely the clinical VT that he'd been having. So what do we think about this tachycardia? Great. Yeah, we can probably stop it there. So that's great. So you can, I think that folks have a pretty good idea of where they're seeing this coming from. I think this is a right bundle configuration, right? It's positive all throughout the precordium, so that puts it back quite basal. It's still inferiorly directed, but maybe not quite as leftward. And so that's most consistent with the aortomitral continuity. It's not always the case that you would find it there, but I think that that's probably the most consistent. If we go back to our little figure here, that's kind of the area that we're talking about with a little right bundle. And then if we think about where the other VT morphology is located, these are the two sites that we're looking at. I think the other thing to keep in mind is when we talk about site of origin, we're usually talking about an idiopathic VT that has its site of origin from one location. When we're talking about a scar-related arrhythmia, it's a little bit different because we're thinking that there might be a reentrance circuit and an exit, but the critical parts of the circuit might be located remotely. So it's possible that there's some scar tissue somewhere between these that's potentially the critical area for both of these VTs. So here's my voltage map that I made of the right ventricle. And you might see that it looks quite a bit, this is the bipolar map on the left and the unipolar map on the right. And you might notice that the low voltage area here matches a lot like what we showed you in the Lamin paper where we found VT exits. And so the low voltages here had some fractionation and late potentials. And then when we looked at the unipolar voltage, so unipolar voltage can give you a wider field of view and can potentially identify intramural substrate if you're looking at the septal side or epicardial substrate if you're looking at a free wall site. But here's kind of that parahysian area. You see that there's some low voltage right around where you'd expect the hys bundle to be measured. And then some potentially some periannular scar as well. And the unipolar voltage is not perfect, particularly up at the annulus, but it at least gives you a suggestion that there might be something going on in there. So for a case like this where you've got something around the aortic root, I usually come retrograde aortic and map above the valve. And so here's an example of mapping above the valve where you can find some in this patient, there were some low amplitude, long fractionated signals. You can see that they're multi-component. There are some that have very high frequency and some that have lower frequency. But you can, and you can see the patient now is biventricularly paced, which was a bit different from the previous EP study. And you can see that in some of the areas of the outflow track near the commissure between the right and left aortic valve leaflets, you can actually find some extremely late fractionated electrograms, which are very interesting. So when we paste these areas, we basically were able to reproduce some morphologies that were similar to VT1, maybe with just a little bit earlier transition. So left bundle here, inferior axis, but with a long stem to QRS delay. So that's something that's more suggestive of a scar related process, some kind of little channel that has longer conduction over towards the more rightward sites. And then as we paste, we could also see some other morphologies with a different stimulus to QRS interval with a right bundle here and inferior axis. And this is just that VT2 to remind you what that looks like. And you can see that those are very, very similar in morphology. And so whenever I see sites in scar with late potentials where I can paste with different stimulus to QRS intervals and reproduce two different VT morphologies, I always wonder if those are a part of a critical site for both VTs. And looking at the intracardiac electrograms here, you can see that when we're pasting, there's a part of the signal that we're not capturing when we get the left bundle morphology beats. Here we paste, there's a little bit of delay and you see this stuff that's not captured. But when we get the right bundle beats, these are actually captured. So it could be that these different parts could have different components of the late potential are playing a role in the two different VT morphologies. So we ended up doing ablation in that area. So this is a lot of how I set up my typical VT ablations. I'll do an ultrasound map to create a 3D geometry of the left ventricle and the right ventricle. Shown here on the right is the left ventricle. You can see the left coronary cusp here, the right coronary cusp, and those areas where we were seeing the late potentials are just below the valve there. And there's a really a very small low voltage area at the bottom, just below the valve and extending back behind the right coronary cusp. And that's where we delivered most of our ablation lesions. We also did ablation in the right ventricular outflow tract overlying that area. And here's just another view of that. Here's the right ventricle kind of curving over the left ventricle. And it's amazing to me always to see how far leftward that right ventricular outflow tract comes. But this is where we did our initial ablation lesions overlying that scar. Here's the ablation in the left ventricular outflow tract area. Unfortunately, after a lot of ablation in what looked like really good areas, the VT2 is still inducible. So what are our other options? There's several techniques that have been described for reaching deep into the septum, bipolar ablation, alcohol ablation, needle catheter ablation, and then potentially epicardial ablation. Now, one of the things I would like to just mention is that it seems unlikely that we're going to be able to reach this area in between the outflow tracts with epicardial ablation. So probably of these other three, none of them is really wrong, but I probably wouldn't select epicardial ablation as the next step. But what I'd like to say to talk about for the next little bit is can imaging help? And for this patient, we did a cardiac CT. So this is for images from a gated cardiac CT with delayed enhancement images. And the reconstruction was done with a part of a collaboration with the Bordeaux Group. And you can see a lot of different things on this scan. You can see the parts of the ICD, certainly you can see the atrial lead, the right ventricular lead, and the CS lead going off behind there. You can see the coronary arteries. And I think what's nice to see about the coronary arteries is you can see the left main here. You can see how if you were epicardial and you were trying to get to the epicardial surface of this scar region that we're looking at here, that the left atrial appendage really covers over a lot of this area. And there's a lot of large coronary artery in this area. The other thing though that you can see is that there's a septal branch coming off of the LAD that heads right towards the scar region. The other thing that this type of scanning can give you an idea of is the wall thickness and the thickness of the scar tissue. So the thinnest area of the scar is kind of the dark area and the moderately thick areas are the sort of lighter gray. And that also can give you maybe an idea of how much dense scar there is and how much potentially partial thickness scar there might be. And the partial thickness scar may be more likely to participate in some of the reentry circuits. So what we did for this patient was needle catheter ablation. So this is a needle catheter that was developed by Bill Stevenson over a 14-year period, really. It was originally a catheter that was developed for delivery of stem cells to the heart. And it basically has an extendable, retractable nitinol needle that you can irrigate out the tip. You can measure electrograms from this needle. And last year at HRS, we actually two years ago now at HRS, we presented the initial series of patients that we treated with this catheter. These are basically the sites where we ended up doing needle catheter ablation. And you see this really mirrors the area that we're interested in in this particular case that I'm showing you. We were able to improve outcomes at six months of follow-up with two-thirds of the patients free of VT or improved. And a third of the patients had continued VT. They were mainly non-ischemic population. There's also another irrigated needle that's gonna be presented as part of the late-breaking clinical trials tomorrow for the Heart Rhythm Society meeting. So the workflow for this is, so here's basically an LAO projection where transeptal through the left atrium and then into the left ventricular outflow tract area. We have the needle deployed into the septum and we're basically injecting contrast from the tip of the needle in order to see where we have good purchase with the needle. And so we did an ablation lesion in this kind of area. And then we approached it again from the right ventricle. This is looking from a posterior view. This is the tricuspid annulus. This is the mitral annulus. And this is approaching basically directly into the right ventricular outflow tract. And you can see here that there's a contrast injection going over towards the right ventricle. And when we, so if you look, this is just the electroanatomic maps with the voltage removed to make it a little bit more clear. Here you see our first set of lesions. Here's in the right ventricular outflow tract. Here's the left ventricular lesions. And then if we draw a little, a little contour around the contrast that's been delivered and add that to the map, you can see the contrast comes right in this area. So the ablation was delivered between the lesions that we had already given with standard RF. And we're able to eliminate the VT, rendering him non-inducible in the procedure. And he's now five months off of antiarrhythmic drugs as of today. So that's a great outcome for this patient. So I wanted to use that as a segue into talking about how successful are we at catheter ablation for VT overall? So if we look back at published series, mainly in ischemic cardiomyopathy, we see that our success rates are not perfect. We're about, you know, sometimes in some cases as low as 50% to 75% successful at controlling VT in the long run. And how do I think about our success rates? Whenever I think of any catheter ablation procedure, whether it's for atrial fibrillation or it's for VT or for another arrhythmia, it sort of has two components to it. One part is the mapping. And that has to do with identifying the underlying mechanism whether it's focal, is it re-entry, is it Purkinje related and identifying the substrate. Do we understand where the abnormal tissue is that's causing the abnormal signals? And then the second part of it is catheter ablation. So that relates to lesion generation, creating conduction block in your identified target. It's no good if you say, okay, the VT is here, but I can't put my catheter on it, I can't ablate it. So if we think back on these substrate identification techniques that we have available to us with imaging, most of the early work was done with MRI. I remember when I was an EP fellow and we would do VTs in non-ischemic cardiomyopathy, the word on the street was you needed to go epicardial, you would map epicardial and the VT was gonna be out there. And I just remember doing a lot of cases where you would go out there and the VT wasn't out there. It was very confusing. So then there was a paper that was published from Frank Bogan looking at the presence of scar substrate on MRI and where it was located. And he found that for non-ischemic cardiomyopathy, there certainly was a proportion of patients that had epicardial substrate. However, there was a large proportion of patients that had mid myocardial substrate seen here. So this is a patient of ours that had cardiac sarcoidosis. And you can see here that there's a strip of scar going into the mid myocardium between the LV and the RV. It's a really old MRI, but it at least makes the point that that's the case. And a similar thing can be even seen with ischemic cardiomyopathy. Ischemic cardiomyopathy is very interesting because we often don't see the VTs until 10, sometimes 15 years after the initial infarction. But with the advent of PCI and revascularization, we're seeing more smaller scars that are more complex that have more complex scar borders and have more mid myocardial involvement. So I think that that's something very important for us to keep in mind. So here's some further work from Dr. Bogan's group looking at MRI then to guide your ablation. So what if you're like, what if I don't have a needle catheter? What if I just need to figure out what to do? And in this case, what Dr. Bogan did is he took a cohort of patients and performed pre-procedure MRI imaging to identify scar substrate. And he basically, his strategy was to aim at the scar substrate and do these long lesions at high wattage power delivery. And he compared that to a historical control that had no preablation imaging. And at least looking at the success rates in somewhat matched patients, he was able to improve his success rates to about two thirds from only 24%, which seems like it's a strategy that makes some sense. And if he was to compare the long-term outcomes of these patients as well, you could see that there was the survival free of VT recurrence, heart transplant, or death was better among the patients that had the imaging guided ablation. And in a really recent paper that I think is still, it's pre-publication in press, that he's published some further enhancements to the strategy. This was a stepwise approach to intramural VT where they were using MRI to identify intramural scars. And he had a stepwise approach where you identified the scar and did extensive ablation, meaning long lesions and high power catheter delivery to cover the entire scar area, depending on the extent of intramural scar noted on MRI. And again, compared to a historical control, he was able to have really pretty good outcomes, which seems to say that this is a reasonable strategy for targeting the intramural substrate. And the reason this is important, if you think about what you're able to measure with voltage mapping, it's pretty unlikely that you're going to be able to assess scar tissue that's several millimeters away from your catheter in an accurate way with just standard, particularly with bipolar voltage mapping and unipolar voltage mapping is not discreet enough often to identify these small scars. So let's talk for a little bit about reasons for failure of catheter ablation. So suppose, so if we use imaging to identify our target, what are reasons that we might not be able to reach it with standard catheter ablation? So we just talked about how VT circuits in the scar might be deeper, the substrate might be deeper than can be reached by standard catheter ablation. Then in addition to fibrosis, other scar components can impair delivery of the ablative energy into the tissue. There can be fat, there can be calcification, and then there can be laminated thrombus. This is a patient with an old antero-apical infarction that has a thrombus that would prevent you from reaching the scar substrate if this is part of the scar substrate. You can also see that portions of that aneurysm are calcified. So imaging can help us identify these substrates and get an idea for what we're gonna have a difficulty with and whatnot. So what if I don't have an MRI, you might say? So here's an example of using intracardiac ultrasound to identify mid-myocardial scar. So here we have an intracardiac echo probe located in the right ventricular outflow tract. We're looking at the left ventricle. We can see the bases of the papillary muscles. We can see the mitral valve over here. But if you look at the lateral left ventricle, you see this bright stripe, and you can actually see areas, let me pause it for one second. You can see some myocardium on the epicardial to the stripe, and you can see some myocardium endocardial to the stripe. So this is something where you can try to identify mid-myocardial scar just based on your ultrasound images and not have to get good fidelity MRI. I actually use a lot of intracardiac ultrasound in my ablation procedures. I wanted to just put a little plug in for that. I think it's really, really helpful to do a full survey of the entire left ventricle and try to, left and right ventricle in some cases, but in this case, the left ventricle, to try to identify both the anatomic portions of the area. You can identify wall thinning. You can identify mid-myocardial scarring. You can even identify sometimes epicardial scarring on intracardiac echo. I found at our institution that I don't get very good fidelity MRI images, and so I've been turning more and more to arterial enhanced CT, and that's what we used in the sarcoid patient that I presented at the beginning of the talk. CT has a lot of advantages. It can be a little bit easier to get good fidelity images in patients with devices. You can see that there's still some problems with artifacts from the leads and such, but some of the areas where we're looking for late enhancement, you can actually still see the mid-myocardial enhancement that you might be interested in your patients with non-ischemic cardiomyopathy. In addition, you get a lot of anatomy, as we talked about in that initial case. You can see trabeculations really well. You can see wall thinning. You can see other parts of the heart, so you can see the coronary arteries and their course. You can see the phrenic nerve. There's a lot of benefits to having that anatomic modeling. You get a good idea of where the coronary course is, where there might be branches of the coronary venous system that could potentially be targets for either measuring electrograms or targeting your catheter ablation. Additionally, you can look at wall thinning here, which can sometimes in the non-ischemic population be discrepant from the areas of scar tissue. You can also identify intramural fat, and you can identify areas of fibrosis, and this is a patient with non-ischemic cardiomyopathy that has this fibrosis, again, in that basal septal area, and you can see it follows the LED so closely. It would be really hard to be epicardial and safely ablate this area. When we get those images, the way we register them in the EP lab is again using intracardiac ultrasound, and so this is just an example of looking at the aortic root with ultrasound. You can usually delineate all the valve cusps. You can look at the coronary arteries, and so we use those then to register the CT image when we do our ablation procedure. And here's for that case with the LED running over the scar tissue area, but this is the area endocardially where we were able to interrupt this patient's PT. So let's talk about some other alternative strategies for delivering energy to the heart if we have mid-myocardial scar. So what we've been talking about in Dr. Bogan's papers is unipolar ablation, which Dr. Sauer spent a lot of time talking about a few weeks ago, where you have an ablation catheter at a dispersive electrode somewhere on the body surface, and you deliver ablation to the heart. And in bipolar RF, you basically are, one of the electrodes, you have two ablation catheters, and one of the ablation catheters basically acts as the dispersive electrode, and you end up delivering RF across the septum in that way. And here's just a comparison in an animal model of two unipolar lesions and then a bipolar lesion, and the thought is that you actually get more heating in the area between the catheters, and you end up with a bigger lesion, at least in normal tissue. There have been some, this requires some special cable hookups to allow the RF generator to accept the catheters, but it's certainly possible to deliver large lesions in normal tissue. There's a little bit of a issue if there's a lot of scar on one side compared to the other, that you might get something more resembling a unipolar ablation lesion on the other side. The other problem is in some IDE studies, there's been a small signal of a safety issue, and that may be just because settings have to be titrated, but one should be aware that steam pops are potentially a dangerous problem with this when it's delivered in a free wall site as opposed to a septal site. Then there's simultaneous unipolar RF, which is similar, but you use two generators and two catheters, and this is just a picture from a recent paper from the Penn Group showing the setup for a simultaneous unipolar. In this case, they used two irrigated ablation catheters and were able to successfully treat six patients with non-ischemic cardiomyopathy. They used long lesions. It's important to note three to five minute applications in order to get persistent suppression of VT. And the first description of simultaneous unipolar was by Yamada and colleagues, and they used an eight millimeter catheter for one of the catheters, and then a 3.5 millimeter irrigated catheter both with cutaneous electrodes. And they had reasonable success with initial VT suppression, but there is a signal of late recurrence with this technique, so it could be that the lesions are not quite as big with simultaneous unipolar. And we talked a little bit about the needle catheter. Here's just another view of it, and I just wanted to show you what the lesions look like from that catheter. Here's a little chart from an initial paper from John Sapp from a few years ago. This green is a standard catheter, and you irrigated standard catheter ablation lesion. The x-axis shows you how deep we are in the myocardium, so a typical lesion maybe will have its peak depth about two to four millimeters below the surface. If you take the needle and just stab it into the tissue and deliver RF through it, all you get is a very, very skinny lesion. It goes pretty far in, but it's not very wide. And once you irrigate it, you actually get a more almond-shaped lesion like this, where you have relative tissue sparing at the surface and you have relative tissue sparing deep, but you get a very wide lesion at the belly. So what are some other techniques that we might use? This is a patient of mine from a few years ago with a non-ischemic cardiomyopathy from Lamin cardiomyopathy. And I just wanted to show you, we did a transcoronary ethanol ablation on him at one point during his course. He's actually subsequently had simultaneous unipolar ablation and then needle catheter ablation, and that bridged him to a heart transplant. So he's currently transplanted. But this is one of his early BT catheter ablations that we did where he had three different VTs. This is, again, Lamin cardiomyopathy with this very familiar now scar in the periaortic area near where you'd expect the his bundle to be. He already had heart block because of his Lamin cardiomyopathy. He had these three VTs. We were able to eliminate two of the VT morphologies, but this one remained after standard catheter ablation in the periaortic area. So this one was kind of incessant and causing him a lot of trouble. So where do you think this one is from? Usha, there's been a couple of questions that have come through. Oh, sure, yeah, absolutely. So a couple of things just related to needle ablation. One was, are you guys performing that in the same sitting or is it a second procedure? And how many times do you stick when you end up using the needle? Right, right. So as part of this, this needle catheter is still under IDE and the requirement is that the patient has to have failed one previous catheter ablation and they cannot have epicardial ablation at the same time as the needle catheter ablation. So oftentimes these are folks that are referred from an outside hospital after an unsuccessful ablation anyway. But so we're usually doing both needle catheter ablation and standard RF for those redos. We're allowed to do both, but we're not doing epicardial ablation. And in terms of the number of deployments, I think our early cases, we did a lot of deployments because we didn't really understand where to go, to be honest with you, for a lot of these VTs. And I think with advances, we did our first case in 2016. And I think as the imaging, which is really, I feel like with CT in particular, taken a huge leap forward recently, we're using a lot more imaging as an adjunct to help us know where to go. And so I would say for my recent cases, I've probably done between five and seven needle deployments because we've known more where we need to go for the catheters. But our early cases, especially the ones with very, very extensive disease, we did a large number of deployments. We haven't seen any complications just related to the needle deployment itself. Okay, great. And then there was some questions from a little earlier. Your technique for pace mapping, specifically what's being asked is, do you ever use unipolar to avoid anodal capture? And if you could comment on your use of half normal saline. Yes, so we actually use all, or at least I use all unipolar pacing. So we use a specialized His catheter that has an indifferent electrode that sits in the IVC and we do unipolar pacing to avoid anodal capture. And it's also, it's really helpful just to make sure you're capturing a very small area of myocardium. It helps with your electrogram fidelity as well. And half normal saline I think is really useful as well. It gives you a little bit larger lesion formation. It hasn't been investigated in some of these prospectively in like an image guided mid myocardial approach, but that's almost certainly what you're doing if you were to use half normal saline. I think one of the caveats with half normal saline is just to make sure that you're aware that steam pops can occur with that as well. And to just be aware of that. And maybe Dr. Sauer at some point might wanna make a comment about that because I'm sure that he mentioned it in his talk. Okay, great, thanks. I put up the poll results there. Yeah, so very interesting. So I put this up as sort of a, there is no answer kind of question. I apologize for that a little bit, but Moderator Band, I like, I like that answer. So let's just take a little look at the morphology here. So it is left bundle. What I would say is there's a little funniness about the left bundle though. It's got this isoelectric segment first. Like if we look at the beginning of the QRS complex in leads two and three here, you can see that there's this isoelectric part in V1 before it becomes left bundle. So that to me pushes it off of just like a little bit into the septum. So thinking about things that get you into the septum might be reasonable. And then otherwise there's a fairly late transition that's consistent with like a right ventricular site. It's inferiorly directed, but definitely not as high as some of the other VTs that we looked at earlier today. And it's positive in one. It's sort of isoelectric a bit in AVL. So I'm worried about it being septal based on this isoelectric start to the QRS in V1. But I think the RV parahysian area is not a bad thought. I think that the right coronary cusp, you could make a strong argument for it. It can look very much like parahysian pacing from the posterior aspect of the right coronary cusp. And that can come very close to some of these septal scars. And the moderator band is the secret sneaky thing that can also exit into the septum and gain purchase into the conduction system. So I think thinking of all of those things is right. I don't think that this VT is characteristic of any of those locations. I think it's probably not consistent with the tricuspid annulus or the mitral annulus. And so this patient, we knew where his scar was located. We knew he had a big septal scar and we were worried about this. We had already tried to ablate on either side of the septum and not gotten it. So we actually were prepared to do alcohol ablation. So here we did an angiogram of the LAD and we were able to identify a couple of septal. Some of them are teeny teeny and there's one that's a big branching one here coming off of the LAD. And this is just my ablation catheter sitting in the right ventricular outflow tract. Oh, sorry, let me just point out the ramus. There's a little ramus right here too. So the first coronary that I work with one of our interventionalists that we engaged was the ramus branch. And this is just a little video that when we hooked up in those coronary views, I think it's really hard to get an idea for where exactly your branch is going. And so one of the things you can do is hook the wire up to your mapping system to get an idea for where it's going. Because when you look at it here, it looks like, oh, maybe it's going somewhere that I want. But when you look at it superimposed on your map, you see that it's going way too lateral. So I think that's really helpful. The other thing you can do is pace from your angioplasty wire. So this is pacing from the ramus. And you can see that you're getting a leftward type of QRS compared to the QRS of our VT that's got a bit more R wave in V1. It's not miles away, but it's a little too high and it's a little bit, it's got this earlier transition leftward than with the R wave in V1, V2, and V3. Then if we go into that first little septal here, you see I have a very patient interventionalist, and then into the second septal here which is that big branching one. You can see here, I sort of, I didn't have them at the same time, so I made a still image here. You can see that both of these guys are kind of heading in the direction of the scar that we've identified from our endocardial map. And so here's pacing from the first septal. And we see now that we're a bit more left bundle than we were with the ramus, right? And when we pace from the second septal, we actually get something looking a bit more left bundle. It's still not perfect, but it's going a lot closer to where we're interested in for our VT. The problem that I've had with these types of alcohol ablations in reinducing the VT with those wires in place is the interventionalist spends a lot of time getting a wire into these tiny little branches and the VT can destabilize the wire. So we haven't done a lot of induction. We've sort of done balloon occlusion and attempts at reinduction after that instead of ablating during VT. But here you can see sort of the final picture of the LAD where that second septal is now gone. And this controlled VT for this patient for about six months or so, Lamin is very progressive. And I think one of the important things that we showed in our VT series from the Lamin group is just that once they start having a lot of monomorphic VT and reduced ejection fraction, it's important to start considering them for advanced therapies and transplant because that's eventually where they're headed. And then the last case I wanted to show you is a patient with an EF of 40 to 45%. We thought he had potentially burnt out sarcoid. He has some scar in his basal, infralateral basal anteroseptal walls. And he had been taken for a number of ablations in the past at an outside hospital. He'd had a VT from the basal septum, peri-aortic areas in the years before. And then he was ultimately maintained on amiodarone and couldn't be weaned from amiodarone without having incessant VT. So he was referred for catheter ablation and here's his VT morphology. So what do you think about this one? Usha, a couple of questions about ethanol ablation. Do you ever use the venous septal perforators? Yes, I should have mentioned that. I don't personally have experience with that, but Dr. Valderrano's group has done it a lot. I think the things to be worried about both with arterial and venous alcohol is to be worried about collaterals. One of the things that our interventional does for the arterial alcohol administration is you really wanna make sure that when the balloon is occluded and you inject contrast, you don't inject collaterals to other circulations because I think one of the worst things you can do with this type of ablation is get uncontrolled alcohol in some other distribution and reduce their EF further, especially for some of these sick cardiomyopathy patients. But there is some data on using the coronary branch, the coronary venous branches also for alcohol. I worry a little bit more that those are prone to collateral formation, which is why I haven't done it as much myself. I always think of those angiograms that we shoot as part of a CRT implant where you do a balloon occlusion of the CS and inject it, you can see the entire heart light up with all the different branches. And so I'm a little worried that there's a potential for that, but there's definitely some experience with that, both in the middle cardiac vein and in the AIV branches. And then there was just a question about specifically what wire are you guys using in those small branches? Yeah, so I actually, I know that there's, is it a biotronic wire that's specifically available or for pacing that you can use for CRT implants? But what we've just used is a standard, my interventionalist usually needs a coded wire to get into these teeny little branches and he worries a lot about thrombus. So I usually use whichever wire the interventionalist wants and then what you have to be aware of is that whatever the coded tip is not gonna be, is there, is not gonna be represented by the pacing. So it's wherever the wire becomes more bare, more proximally is where you're gonna get your pacing from. Okay, great. Okie doke, and so most everybody said left infrared septum, this was probably too easy, this one. So this one I didn't think was gonna be a very difficult case, to be honest with you. It's a narrow VT, right, has a right bundle. It's positive in V2 and V3 and then it becomes negative V4 through V6. So, and then it's superiorly directed, negative in two and negative in three and septal because it's positive in one and positive in AVL. So that kind of puts it in this left ventricular in infrared septum, kind of at the mid ventricle, halfway down, kind of where you might go looking for an idiopathic fascicular VT. So I thought, great, this is not, it doesn't look slurred, it doesn't look evil in any other way. I thought it was gonna be easy. And it turned out it really wasn't. So here's the voltage mapping that we did for this patient. So remember, his EF is really pretty good. It's almost preserved and you can see that on bipolar mapping, he had a periaortic scar and the unipolar mapping suggested that there might be a more extensive abnormality, more septally. So when I mapped him during VT, this was the earliest activation we could get and it really appeared very much like a focal VT. We mapped all, this was the earliest spot. It all seemed to be centrifugally going away from the spot. You can see the unipolar electrogram here is very QS. It's early, but not super early. The blood pressure's not great, but you have a little bit of time to do some mapping. And so we ablated there and nothing happened. So ablated for a long time in that spot. It looked like it should be good and then we got no termination, so what to do? So for this, we did the simultaneous unipolar because at the time we didn't have a setup for bipolar ablation. And one of the things you can see may have been a problem for this case. So what you see is we're transeptal with one catheter here, the irrigated catheter. We have an eight millimeter catheter in the right side going up against the septum. The distance between these catheters is fairly large. So when this starts to get to be above a centimeter or so, it's unlikely that the unipolar ablation is going to, any bipolar ablation actually, whether simultaneous unipolar or bipolar ablation is going to have a transmural lesion. If the electrodes are so far separated. So here we ablated, we got termination, we couldn't reinduce, so we were really happy. And then the amiodarone was stopped, but he recurred with VT four weeks later. So I'm guessing we got a little bit of edema in the septum and it probably went down over the four weeks and then the VT came back. So we bottomed back for needle catheter ablation. This is one of the early needle cases that we did. So we can, you can see the approach is very similar to where we were just using it for the simultaneous unipolar. Here we are in the left ventricle pointing at the septum. And I just highlighted where the needle would be because some of these, the x-ray pictures don't show the needle location that well. So that was great. When we paste from the needle intramurally, we got something that looked a lot like the VT. So that was reassuring. Also during VT, we got some nice early signals on the needle, but not on the rest of the catheter, which is usually a good sign with some nice QS unipolars. And so we delivered RF and it initially cut the cycle length of the VT and we got this funny rhythm afterwards that was a bit like a junctional type of a rhythm, slow, similar, but not exactly the same in morphology as the VT before. The axis is a little bit different. But then this died out after, you know, several minutes. He sat in this VT and we watched it and then it slowed. That went away. And then we were able, we weren't able to induce VT again. So we were happy. Once we were in sinus rhythm, here's what the pacing from the needle looked like. It looks just like the VT. So we delivered a few more lesions just for good measure. There's a little bit more of stim to QRS delay here, maybe just a touch. So maybe there's some mid myocardial scar that we were accessing. And this is what the needle lesions looked like from the right side and from the left side. You can see the intraventricular septum is a little bit generous here. So it's, there's quite a distance covered there. Here's an intracardiac echo showing the needle lesion generation. But one week later, incessant VT again. Now what? What is going on? So this VT looks very similar to the VT that we had initially. But this time, when I went back into MAP, I found a beautiful, super early site where I terminated VT very early. So what's going on? Did I miss it the whole time? Did something change? And he's now 36 months after his ablation off amiodarone without recurrent VT after this one. But this is standard RF, this last one. So what's going on here? It's a deep intramural, likely small scar. And here we think the final recurrence was almost certainly due to surface sparing. So the needle lesion is almond-shaped, spared the surface a little bit and kept us from getting transmurality. The last lesion, you know, that was delivered from the standard RF catheter just completed that transmurality. But I don't know, is the mechanism of this tachycardia reentrant or focal? The mapping looks focal. Potentially appears to be playing a role because of that funny automaticity we got with termination of the tachycardia. But if it's reentry, where is the circuit? And how can this circuit supported be so slow? It's very strange. So I just wanted to leave you guys with some ideas, the future directions of looking at intramural VTs. There's a really nice paper from Rod Tongue looking at simultaneous endocardial and epicardial mapping to try to work out some of these VTs that look focal on either side of the septum, but maybe have reentry midmyocardialy. There's some interesting experimental work characterizing the Hisperkinje system and fiber orientation in scar that may help us understand how you can get circuitous conduction in the septum and get slower VTs when the scar is very, very small. And then of course there are other methods of ablation energy delivery, even non-invasive ablation that may be helpful for some of these patients. And I thank you for your attention. Thanks so much, Usha. You've gone through most of the questions that came through the chat. If anyone has other questions, you can feel free to unmute yourself and ask. I guess one of the things that a lot of people have been wondering is endpoints for ablation can be very difficult in this patient population. I guess what's your ideal endpoint and what are you satisfied with when you're done with one of these procedures? I think it's really tough. And I think one of the reasons is in the non-ischemic population, one of the troubles we've had is like, if you look at that 30% of people that were not successful with needle catheter ablation, a lot of those folks were non-inducible in the lab. So I think the problem is that I think a lot of our non-ischemic population may have focal VTs that we don't know about, or we just aren't able for whatever reason to generate their VT when they come to the lab, even though they have a lot of VT. So I do a lot of substrate-based work. I think for patients that I'm suspecting that they have mid-myocardial substrate, I do a lot of imaging. I try to target the imaging as much as I can. Obviously, inducibility is important. I'd love to see the VT terminate if I can. But, and I do program stimulation at the end. But I think for these intramural circuits, what's really difficult is that you don't see a lot of the substrate on your catheter. So knowing an endpoint is very difficult. So like, if you look at Frank Bogan's paper where he was doing the stepwise approach, he's aiming at the substrate and he's targeting some impedance drops and lengths of lesions, but he's not targeting an electrophysiologic endpoint. So I think this is something that's gonna challenge us in the future to look for better endpoints for our ablation procedure to know when to stop for these patients. Because it's okay when they have a teeny little scar like this, but if there's a very large, very extensive scar, it can be very challenging. Usha, that was a fantastic talk. And we're so proud of all the work you've done. It was really great to see it. I wanted to see whether or not you could talk a little bit about this last sentence and what your experience is with SBRT for treating mid-myocardial substrate. And what specifically, all these people have mapping, what is it about their substrate that would be something that would tilt you towards that approach? Right, I think that like the failure of catheter ablation for VT from a substrate standpoint falls into two camps. There's the people that have a teeny little scar that we can't reach that's in some very potentially dangerous area near a coronary or something like that. That's a tough area for me for SBRT because I worry that we might have a risk of damaging a coronary if we ablate too close to it. But people who have very extensive scars, sometimes I call it crossing the Sahara Desert on a pogo stick. You have a huge scar and you're going with point by point by point ablation, you're never gonna be able to address all of the late potentials and eliminate all of the arrhythmogenic substrate. That is a great target, I think, for SBRT. There's a little bit of a signal that when the substrate gets too big, there may be an amount of radiation you might not wanna deliver to the heart. But we had especially one very interesting case of a gentleman with a post-infarct VT. The infarct was very old. The guy had his infarct when he was 30. And the VTs showed up in a patient in his 70s. And there had been a huge amount of fatty metoplasia of the infarct. And we couldn't deliver good RF energy into the scar. And with the needle, with anything, we could sometimes get VT termination, but the signals looked great, but we could never get effective persistent block. That patient did extremely well with SBRT. I think that's something where SBRT really outperforms RF ablation on a pretty routine basis.

ventricular tachycardia

VT ablation

case studies

origin of VT

substrate of VT

localization techniques

ablation techniques

imaging guidance

alternative energy delivery methods

future directions